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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between November 1 and 22, 1985, an outbreak of acute, nonbacterial gastroenteritis occurred in a 600-bed hospital in Toronto, Ontario, Canada. Illness in 635 of 2,379 (27%) staff was characterized by fatigue, nausea, diarrhea, and vomiting and had a median duration of 24-48 hours. The finding of virus-like particles measuring 25-30 nm in six stool specimens and low rates of seroresponse to Norwalk virus (3/39) and Snow Mountain agent (1/6) suggest that a Norwalk-like virus was responsible for the outbreak. The outbreak was of abrupt onset and high incidence, affecting 79 people in a single day. No common food or water exposure could be identified. The attack rate was greatest (69%) for staff who had worked in the Emergency Room. Of 100 patients and their companions who visited the Emergency Room on November 11-12 for unrelated problems, 33 (33%) developed gastroenteritis 24-48 hours after their visit, versus 0 of 18 who visited the Emergency Room on November 8 (p less than 0.001). An analysis of housekeepers who worked at least once during the period from November 9-13, which included those who became ill during the period of November 9-14, showed that the risk of becoming ill was four times greater for those who visited or walked through the Emergency Room than for those who did not (p = 0.028). These data are consistent with the possibility of the airborne spread of a virus.
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PMID:25- to 30-nm virus particle associated with a hospital outbreak of acute gastroenteritis with evidence for airborne transmission. 283 99

Water deprivation (WD) resulted in increased serum osmotic pressure (OP) and decreased body weight (WB); adrenal aldosterone content did not change. Adrenal corticosterone content tended to be elevated during early WD, indicating a stress response, but tended to decrease after seven days of WD, suggesting adrenal fatigue. During water restriction (WR), after the period of weight loss, adrenal corticosterone content and serum OP were elevated. As the birds began to gain weight, aldosterone levels did not change but adrenal corticosterone content and serum OP approached control values, suggesting that the birds were beginning to adapt to the WR. Adrenal sensitivity to ACTH was indicated by the elevated adrenal aldosterone and corticosterone content after ACTH injection.
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PMID:Adrenal responses to chronic and acute water stress in Japanese quail Coturnix japonica. 285 51

We have recently demonstrated that humans report heat stimuli as less painful when presented concurrently with a second noxious stimulus applied to another part of the body. Previous neurophysiological studies have shown that similar heterotopically applied noxious stimuli selectively and completely inhibit the activity of wide-dynamic-range (WDR) neurons in the dorsal horn - a phenomenon termed diffuse noxious inhibitory controls (DNICs). Taken together, these 2 lines of evidence suggest that activation of WDR cells may be necessary for normal perception of pain. Recent studies in the behaving monkey have additionally shown that WDR neurons respond to small changes in noxious heat stimuli better than do high threshold neurons, thus indicating a more specific role for WDR neurons in sensory-discriminative aspects of pain perception. If DNICs do indeed selectively and completely inhibit the activity of WDR neurons, then a heterotopically applied noxious stimulus should selectively interfere with a subject's ability to discriminate noxious stimuli. This hypothesis was tested using a noxious heat discrimination task and a cold water (5 degrees C) diffuse noxious stimulus. We found that the ability to detect small changes (0.4-0.8 degrees C) in painful heat stimuli applied to the face decreases when the person's hand is submerged in painfully cold water (P = 0.005) and that this effect persists, to a lesser extent, after the hand is removed from water. Control tasks, using visual stimuli, demonstrated that the modulation of nociceptive discrimination was not a generalized effect on sensory perception; other control measures indicated that the results could not be attributed to distraction, fatigue or changes in response bias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of diffuse noxious inhibitory controls (DNICs) on the sensory-discriminative dimension of pain perception. 291 3

Two indices of the total mechanical load on the ventilatory muscles, i.e., the work per minute (W.min-1) and the inflation pressure time index (PTI), have been developed to better assess muscle energy demands and fatigue potential. However, the relationship of these two indices to the various individual determinants of load and to muscle energy demands and fatigue potential are not well understood. To investigate these relationships in a theoretical fashion, we first constructed a computer model to quantitate the magnitude and relative effects of changes in the ventilation component of load, i.e., alveolar ventilation demands (VA) and dead space volume (VD), and changes in the respiratory system impedance component of load, i.e., compliance (Crs) and resistance (Raw), on W.min-1 and PTI over a wide, clinically relevant, range of ventilatory conditions. From this analysis, we demonstrated that: (1) high mechanical loads could be developed over a wide range of circumstances (i.e., W.min-1 ranged from 0.29 kg.m.min-1 to 30.55 kg.m.min-1 and PTI ranged from 1.22 to 28.8 cm H2O as ventilation increased from 7 to 39 L.min-1 and impedances worsened from normal to a combined restricted and obstructed pattern); (2) each load determinant (i.e., VA, VD, Crs, and Raw) contributed substantially to these two indices of total mechanical load; (3) although impedance changes had comparable effects on W.min-1 and PTI, ventilation changes, as would be expected, had a greater effect on W.min-1 than on PTI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanical loads on the ventilatory muscles. A theoretical analysis. 293 74

The effect of a sustained-release aminophylline preparation on diaphragmatic contractility was investigated in patients with stable chronic obstructive lung disease (FEV1 = 22.6% of predicted value). Ten such patients were tested before (control) and after a week's course of oral aminophylline. Diaphragmatic contractility was evaluated by measuring the transdiaphragmatic pressure generated at residual functional capacity by bilateral electrical stimulation of the phrenic nerves. The nerves were stimulated supramaximally at 1 Hz, using needle electrodes. Plasma aminophylline levels (12.5 +/- 0.9 mg/l) were within therapeutic range in all patients. After treatment with aminophylline, for each stimulation the transdiaphragmatic pressure increased significantly from 14 +/- 1.3 to 17 +/- 1.3 cm H2O (+21%; P less than 0.005). These results confirm that aminophylline increases the force of contraction of the diaphragmatic fibres electively tested by the technique used. Long-term treatment with theophylline in therapeutic doses may be of interest in such patients, as it might improve their diaphragmatic contractility and result in better control of both respiratory muscle fatigue and episodes of acute respiratory failure.
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PMID:[Action of aminophylline on the strength of contraction of the diaphragm in patients with chronic obstructive respiratory insufficiency]. 295 24

Daily administration of dithiobiuret (DTB, 1 mg/kg X 6 days, ip) produced delayed onset muscle weakness in rats as indicated by failure in a treadmill test. In nerve-muscle preparations from DTB-intoxicated rats neuromuscular toxicity was manifested as contractile fatigue during tetanic nerve stimulation. As muscle weakness developed, feed intake decreased and the animals lost body weight. Water intake was not altered during this time, but urine output was increased concomitant with the development of muscle weakness and resulted in a state of negative water balance. Daily administration of d-penicillamine (d-PEN) antagonized DTB-induced treadmill failure in a dose-dependent fashion. A daily dose of d-PEN (1 mMol/kg, ip) that completely antagonized treadmill failure also antagonized the contractile fatigue, reduced feed intake, weight loss and negative water balance caused by DTB administration. In rats already intoxicated with DTB, initiating daily d-PEN treatment or discontinuing further DTB administration, caused the animals to recover normal treadmill performance after a latent period of five days. A single dose of d-PEN (1 mMol/kg, iv) was not effective in reversing treadmill failure or contractile fatigue in rats already intoxicated with DTB. Thus, continuous daily administration of d-PEN was necessary for it to be effective. A single dose of d-PEN (1 m Mol/kg, ip) administered one hr after [14C]-DTB (1 mg/kg, ip) did not affect the plasma and tissue concentrations of DTB-derived radioactivity or their corresponding elimination kinetics. Cumulative urinary and fecal excretion of DTB-derived radioactivity were also unaffected by d-PEN administration as were the relative proportions of DTB and two of its metabolites, monothiobiuret and thiuret, in urine. Other agents that produced dose-dependent antagonism of DTB toxicity were diethyldithiocarbamate, disulfiram, cysteamine and 2,2'-dipyridyl. Considering the chemical and biological properties of DTB and its antagonists, a mechanism of antagonism involving an alteration of the thiol-disulfide and/or divalent metal cation status of motor axon terminals is postulated.
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PMID:Antagonism of dithiobiuret toxicity in rats. 301 25

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
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PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

A case of hyponatremia is presented with water intoxication due to treatment with oxcarbazepine (OxCZ). The patient was admitted because of exceeding dullness and increasing seizures. Low values for serum sodium and osmolality were found. Simultaneously with the reduction in OxCZ, values of sodium and osmolality increased, normalizing on discontinuation of the drug, and the exceeding tiredness as well as the generalized seizures disappeared. Low values of arginine-vasopressin were found, suggesting that the mode of action of OxCZ was directly or indirectly at the level of the kidney.
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PMID:Hyponatremia induced by oxcarbazepine. 314 48

A 58-yr-old woman presented with recurrent chest infections, breathlessness, and orthopnea. She complained of nonspecific tiredness and aching limbs. A chest radiograph showed an elevated right hemidiaphragm. Thyroid function tests showed her to be severely hypothyroid (T4 = 23 nmol/L; TSH greater than 50 mU/L). Measurement of maximal respiratory mouth pressures (expiratory: 50 cm H2O, normal, 94 +/- 33; inspiratory: 15 cm H2O, normal, 71 +/- 27) suggested global respiratory muscle weakness. Severe bilateral diaphragm weakness was demonstrated by a greatly reduced maximal transdiaphragmatic pressure (Pdi) (Pdi Pimax = 0, normal, 65 +/- 31 cm H2O; sniff Pdi = 25 cm H2O, normal, 121 +/- 25). No Pdi was detectable on stimulation of the right phrenic nerve, whereas, on the left, it was 11 cm H2O (normal 7 to 15 cm H2O). Phrenic nerve conduction time was prolonged to both sides (right, 12 ms, left, 10 ms; normal, less than 9.5 ms). The relaxation rate of Pdi after a maximal sniff and after bilateral phrenic nerve stimulation was abnormally slow (7.4%/10 ms, 6.3%/10 ms, respectively). Three months after starting treatment with thyroxine she had become euthyroid, and phrenic nerve conduction times and Pdi relaxation rates had returned to normal. Maximal respiratory pressures, vital capacity, and maximal voluntary ventilation improved progressively on treatment, although maximal respiratory pressures still had not reached the normal range after six months. We conclude that hypothyroidism may present with breathlessness due to respiratory muscle weakness and/or phrenic nerve neuropathy and is reversible with treatment.
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PMID:Hypothyroidism presenting with respiratory muscle weakness. 319 39

Exercise is known to produce changes in the amount and distribution of water in skeletal muscle. Because MR imaging is highly sensitive to changes in water distribution, these changes should be detectable under appropriate imaging conditions. Imaging of the forearms and/or legs was performed in 16 volunteers at 0.35 T, before and after exercise. Exercises included finger flexion and extension, wrist flexion, ankle plantar flexion, and great toe extension. In the case of handgrip exercise, the level of exertion was quantitated. Individual muscles were frequently indistinguishable on preexercise scans. After exercise, active and inactive muscles could be clearly distinguished. For example, in the flexor digitorum profundus, finger flexion resulted in an increase in the image-derived estimate of T1 (T1 postexercise was 1037 +/- 162 msec vs T1 preexercise of 590 +/- 49 msec, p less than .001). T2 also increased (T2 postexercise was 35 +/- 2 msec vs T2 preexercise of 28 +/- 1 msec, p less than .001). Relative spin density also increased (p less than .001). T1, T2, and spin density subsequently decreased with time but were still increased above baseline at 10 min postexercise (p less than .005). Signal changes correlated moderately with the level of exertion (r = .63) and fatigue (r = .45). Vascular occlusion did not prevent intensity changes. Thus, changes in skeletal muscle MR signal intensity occur with exercise and appear to parallel known alterations in water distribution.
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PMID:Acute effects of exercise on MR imaging of skeletal muscle in normal volunteers. 326 Jul 16


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